ArticleCancer cell international2026
Novel role of the class II α-isoform of phosphatidylinositol 3-kinase in hepatocellular carcinoma: suppressing metastasis by targeting Wnt/β-catenin signaling via inhibiting phosphorylation of LRP6.
Article in Cancer cell international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Hepatocellular carcinoma (HCC) is one of the most lethal cancers worldwide because of metastasis. The class II α-isoform of phosphatidylinositol 3-kinase (PIK3C2A) was found to be a regulator in proliferation and migration of endothelial cells, but its role in cancer metastasis has less been evaluated. In this study we find it functions as a tumor suppressor. PIK3C2A was frequently down-regulated in human HCC cells and tissues. Low PIK3C2A expression correlated with elevated LRP6 phosphorylation, β-catenin nuclear accumulation, and Wnt/β-catenin hyperactivation in clinical HCC tissues. Low PIK3C2A predicted poor overall and disease-free survival and aggressive clinicopathological features. Loss of PIK3C2A significantly promoted HCC cells invasion and migration in vitro, and promoted tumor growth and metastasis in vivo. And these changed phenotypes by PIK3C2A knockdown in HCC cells could be rescued by exogenous expression of PIK3C2A. Mechanism studies demonstrated loss of PIK3C2A activated Wnt/β-catenin signaling dramatically. Further investigations showed loss of PIK3C2A gave rise to a decrease in phosphatidylinositol (3,4) bisphosphate (PI(3,4)P
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